Acute kidney injury (AKI)

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You are looking at 1-10 of 17 items for: environmental arrhythmia MED00340 CAR0042

Acute kidney injury (AKI) Simon Steddon, Neil Ashman, Alistair Chesser, and John Cunningham Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199651610 eISBN: 9780191742934 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199651610.003.0002

Definition - Epidemiology - Biomarkers of AKI - Causes and classification - Prevention of AKI - Pre-renal AKI - Causes of pre-renal AKI - Causes of intrinsic renal AKI - Acute tubular necrosis (ATN) - Pathophysiology of ATN - AKI: recognition - AKI: priorities Assessing AKI: clinical clues - Assessing AKI: urinalysis - Assessing AKI: blood tests Assessing AKI: imaging - Assessing AKI: histology - AKI management: a checklist - AKI management: volume replacement—which fluid? - AKI management: volume replacement —how much? - AKI management: hyperkalaemia - AKI management: pulmonary oedema - AKI management: electrolytes and acidosis - AKI management: other strategies - AKI management: nutrition - AKI management: myths - AKI: hope for the future? - Contrastinduced AKI (CI-AKI) - Rhabdomyolysis - Rhabdomyolysis: management - AKI in cirrhosis - Management of HRS - Tumour lysis syndrome - Abdominal compartment syndrome (ACS) - AKI in the developing world - AKI in sepsis - Managing septic shock and AKI - Renal replacement therapy in AKI - RRT in AKI: modalities - RRT in AKI: choosing modality? - RRT in AKI: prescription - RRT in AKI: anticoagulation - RRT in AKI: citrate regional anticoagulation - Peritoneal dialysis (PD) in AKI -

Hypertension Simon Steddon, Neil Ashman, Alistair Chesser, and John Cunningham Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199651610 eISBN: 9780191742934 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199651610.003.0006

Hypertension facts and figures - What is hypertension? - Pathogenesis: general Pathogenesis: genetics, arterial stiffness, and SNS - Pathogenesis: RAS and other factors - BP measurement - Clinical assessment - Classification and treatment thresholds Cardiovascular risk assessment - Lifestyle measures - Secondary hypertension - Primary hyperaldosteronism - Specific causes of hyperaldosteronism - Other ‘hyperaldosteronism’ syndromes - Other causes of secondary hypertension - Drug management of hypertension - Guidelines for drug treatment - BP treatment: special situations - Clinical trials in hypertension - Diuretics 1 - Diuretics 2 - #-blockers - #-blockers - Calcium channel blockers - ACE inhibitors (ACE-I) - A2 receptor blockers (ARB) - Other antihypertensive agents Page 1 of 6 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). date: 27 January 2017

- Non-pharmacological strategies - Resistant hypertension - Hypertensive urgencies and emergencies - Assessing urgencies and emergencies - Management of urgencies and emergencies - Orthostatic hypotension -

The kidney in systemic disease Simon Steddon, Neil Ashman, Alistair Chesser, and John Cunningham Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199651610 eISBN: 9780191742934 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199651610.003.0008

Diabetic nephropathy - Diabetic nephropathy: progression - Diabetic nephropathy: pathology - Diabetic nephropathy: prevention, screening, and assessment - Diabetic nephropathy: management - Diabetic nephropathy: management 2 - Other diabetes-related urinary tract disorders - Plasma cell dyscrasias - Myeloma: cast nephropathy - Monoclonal Ig deposition disease - Renal amyloid: AL amyloid - Renal amyloid: AA amyloidosis Renal amyloid: other forms - Cryoglobulinaemia - Sickle cell nephropathy - The kidney in systemic vasculitis - ANCA-associated vasculitis - ANCA-associated vasculitis: investigations - ANCA-associated vasculitis: treatment - ANCA-associated vasculitis: monitoring response and predicting relapse - Henoch–Schönlein purpura - Polyarteritis nodosa - Churg–Strauss syndrome - Anti-GBM (Goodpasture’s) disease - Lupus nephritis - Lupus nephritis: initial treatment - Lupus nephritis: further treatment - Antiphospholipid syndrome (APS) - Systemic sclerosis - Rheumatoid arthritis - Sarcoidosis - Fabry’s disease - HIV and renal disease - HIV and renal disease: HIVAN - HIV and renal disease: other lesions - Hepatitis B - HBV-related renal disease - HBV and ESRD - Hepatitis C-related renal disease - HCV-related disease: management - HCV and ESRD - The kidney in infective endocarditis - Renal tuberculosis - Renal tuberculosis: TB-TIN and TB in patients with ESRD - Schistosomiasis - Malaria -

Acute kidney injury in polytrauma and rhabdomyolysis Mehmet #ükrü Sever and Raymond Vanholder Print Publication Year: 2015 Published Online: Oct 2015 ISBN: 9780199592548 eISBN: 9780191779145 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199592548.003.0252

The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome. Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular Page 2 of 6 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). date: 27 January 2017

obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crushrelated AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma. In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis. Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia. In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.

Essential urology Simon Steddon, Neil Ashman, Alistair Chesser, and John Cunningham Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199651610 eISBN: 9780191742934 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199651610.003.0009

Urinary tract infection: introduction - Urinary tract infection: investigations and treatment Urinary tract infection: miscellaneous - Reflux nephropathy - Congenital abnormalities of the kidney and urinary tract - Nephrolithiasis - Stone disease: evaluation - Stone disease: management - Acute renal colic - Obstruction: overview - Obstruction: pathophysiology - How to approach obstruction - Obstruction: imaging - Obstruction: treatment - Pelviureteric (PUJ) obstruction - Retroperitoneal fibrosis: overview - Retroperitoneal fibrosis: management - Investigation of a renal mass - Renal cell carcinoma: general - Renal cell carcinoma: diagnosis - Renal carcinoma: management and follow-up - Tumours of the bladder: overview - Tumours of the bladder: pathology and management - Tumours of the renal pelvis and ureter - Benign prostatic enlargement: general - Benign prostatic

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enlargement: investigation and management - Prostate cancer: general - Prostate cancer: investigation - Prostate cancer: screening - Prostate cancer: management -

Renal medicine Elaine Jolly, Andrew Fry, and Afzal Chaudhry (eds) Print Publication Year: 2016 Published Online: Oct 2016 ISBN: 9780199230457 eISBN: 9780191742408 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199230457.003.0017

Chapter 17 covers the basic science and clinical topics relating to ophthalmology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers renal basic science, pathophysiology of renal disease, the kidney as an 'endocrine' organ, renal investigations, acute kidney injury, chronic kidney disease/renal failure, renal replacement therapy, renal transplantation, haemodialysis, peritoneal dialysis, nephrotic syndrome, primary glomerular causes of nephrotic syndrome/proteinuria, rapidly progressive glomerulonephritis, IgA nephropathy, mesangiocapillary glomerulonephritis, tubulointerstitial nephritis, renal tubular disorders, urinary tract obstruction, renal stone disease, urinary tract infection in adults, renovascular disease, renal tumours, inherited renal disease, and renal disease and pregnancy.

Chronic kidney disease (CKD) Simon Steddon, Neil Ashman, Alistair Chesser, and John Cunningham Print Publication Year: 2014 Published Online: Mar 2014 ISBN: 9780199651610 eISBN: 9780191742934 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199651610.003.0003

What is chronic kidney disease (CKD)? - Prevalence of CKD - Diagnosis of CKD Cardiovascular disease in CKD - Pathogenesis of CKD - Progression of CKD: general Progression of CKD: antihypertensives in CKD - Progression of CKD: miscellaneous Advanced CKD: the uraemic syndrome - Complications of advanced CKD - Anaemia and CKD - EPO and the kidney - Erythropoiesis-stimulating agents (ESAs) - Prescribing ESAs - ESAs: additional benefits - ESAs: target haemoglobin - Iron 1: metabolism and markers - Iron 2: therapy and targets - CKD-mineral and bone disorder (CKD-MBD) - CKD-MBD: bone disease - CKD-MBD: physiology - CKD-MBD: clinical features - CKD-MBD: vascular calcification - CKD-MBD: treatment - CKD-MBD: hyperphosphataemia - CKDMBD: vitamin D treatment - CKD-MBD: calcimimetics - CKD-MBD: parathyroidectomy - Calcific uraemic arteriolopathy (calciphylaxis) - Diet and nutrition in CKD - Malnutrition in CKD - Endocrine problems in CKD - CKD management overview - Advanced CKD care - Conservative treatment of CKD: symptomatic management of ESRD - Conservative treatment of CKD: general -

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Nephrology and urology Mark Gardiner, Sarah Eisen, and Catherine Murphy Print Publication Year: 2009 Published Online: Nov 2012 Publisher: Oxford University Press ISBN: 9780199227730 eISBN: 9780191753183 DOI: 10.1093/med/9780199227730.003.0006 Item type: chapter

The urinary system - Clinical nephrology - Urinary tract infection - Glomerulonephritis - Nephrotic syndrome - Renal failure - Congenital anomalies of the urinary tract - Renal anomalies and inguinoscrotal disorders - Cystic disease and tubulopathies - Genetic syndromes and HUS - Hypertension, urolithiasis, and nephrocalcinosis - Case-based discussions

Cognitive function, depression, and psychosocial adaptation Manjula Kurella Tamura, Mark L. Unruh, and Ea Wha Kang Print Publication Year: 2015 Published Online: Oct 2015 ISBN: 9780199592548 eISBN: 9780191779145 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199592548.003.0272

Psychiatric complications of end-stage renal disease are common, often debilitating, and potentially preventable. Patients with end-stage renal disease are at higher risk for psychiatric disorders compared to patients with other chronic health conditions, and those who suffer from psychiatric complications are at higher risk for death and dialysis withdrawal. Both dementia and depression also reduce quality of life and impair adherence to prescribed therapies. In addition, patients with end-stage renal disease are confronted with multiple stressors related to their illness and treatment. This chapter reviews the clinical approach to cognitive impairment, depression, and psychosocial adaptation among patients with end-stage renal disease.

Acute kidney injury in the tropics Vivekanand Jha Print Publication Year: 2015 Published Online: Oct 2015 ISBN: 9780199592548 eISBN: 9780191779145 Item type: chapter

Publisher: Oxford University Press DOI: 10.1093/med/9780199592548.003.0241

The spectrum of acute kidney injury (AKI) encountered in the hospitals of the tropical zone countries is different from that seen in the non-tropical climate countries, most of which are high-income countries. The difference is explained in large part by the influence of environment on the epidemiology of human disease. The key features of geographic regions falling in the tropical zones are climatic, that is, high temperatures and absence of winter frost, and economic, that is, lower levels of income. The causes and presentation of tropical AKI reflect these prevailing cultural, socioeconomic, climatic, and eco-biological characteristics. Peculiarities of tropical climate support the propagation of several infectious organisms that can cause AKI and the disease-transmitting vectors. In contrast to the developed world, Page 5 of 6 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). date: 27 January 2017

where AKI usually develops in already hospitalized patients with multiorgan problems and iatrogenic factors play a major role, tropical AKI is acquired in the community due to issues of public health importance such as safe water, sanitation, infection control, and good obstetric practices. Infections such as malaria, leptospirosis, typhus, HIV, and diarrhoeal diseases; envenomation by animals or insects; ingestion of toxic herbs or chemicals; intravascular haemolysis; poisoning; and obstetric complications form the bulk of AKI in the tropics. Poor access to modern medical facilities and practices such as seeking treatment from traditional faith-healers contribute to poor outcomes. AKI extracts macro- and microeconomic costs from the affected population and reduces productivity. Improvement in the outcomes of tropical AKI requires improvement in basic public health through effective interventions, and accessibility to effective medical care.

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